Thlaspi arvense suppresses gut microbiota related TNF inflammatory pathway to alleviates ulcerative colitis

Wenkai Wang Yiyang Zhao Ziwei Wang Chaowei Wang Ling Bi Yan Wang ^*

• Department of Medical Oncology, Shuguang Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China

Thlaspi arvense (TA), a traditional herb for ulcerative colitis (UC), exerts therapeutic effects through multi-target mechanisms involving gut microbiota modulation, inflammatory suppression, and intestinal barrier protection. In DSS-induced UC mice, TA dose-dependently reduced weight loss, disease activity, and mucosal damage while inhibiting microbial translocation via fluorescence in situ hybridization. ELISA analyses revealed TA balanced pro-inflammatory cytokines (TNF-α, IL-1β, IL-6) and anti-inflammatory IL-10, alongside oxidative stress markers (SOD, MDA). 16S rRNA sequencing demonstrated TA restored gut microbiota diversity, suppressed Escherichia-Shigella (positively correlated with TNF-α), and attenuated infection-related pathways. Network pharmacology identified 220 potential targets, with TNF-α, IL-6, and AKT as central hubs enriched in TNF signaling. Molecular docking and dynamics simulations confirmed stable binding of TA compounds, notably isovitexin, to TNF-α. In vivo, TA inhibited TNF-α/NF-κB pathway activation in intestinal tissues, while in vitro studies showed isovitexin directly alleviated TNF-α-induced epithelial damage. These synergistic actions highlight TA’s capacity to remodel pathogenic microbiota, suppress TNF-driven inflammation, and preserve barrier integrity. The active component isovitexin further exemplifies targeted efficacy against epithelial injury, positioning TA as a multi-scale therapeutic agent. These findings provide mechanistic insights into TA’s host-microbe and intracellular signaling interactions, supporting its standardization and the development of isovitexin as a precision therapy for inflammatory bowel diseases.